Establish a murine model for hyperuricemia (HU) and periodontitis to explore whether there is correlation between them and provide a basis for periodontal treatment.

Fourteen male KM mice were divided into 2 groups; the HU group (n＝7) was fed food supplemented with potassium oxonate and uric acid, the NC group (n＝7) was fed standard food, and the induction period was 35 days. On the 25^th day, the molars on one side were ligated to induce periodontitis (P side), while the opposite was true for the control (C side). Baseline and terminal serum uric acid (UA) levels were detected, and alveolar bone resorption was analyzed by micro-CT.

The serum UA level of HU mice was (112.94 ± 26.82 )mol/L, that of the NC group was (72.21 ± 19.95) μmol/L, and the difference in UA level was statistically significant (P < 0.05). The P side bone volume fractions of the HU and NC groups were( 29.01 ± 11.09)% and (29.56 ± 15.27)%, respectively, which were not significantly different (t＝-0.072, P＝0.944). The P side bone mineral densities of the HU and NC groups were(0.53 ± 0.16) g/cm³ and (0.52 ± 0.14) g/cm³, respectively, which were not significantly different (t＝0.038, P＝0.970). Additionally, there was no correlation between HU or serum UA and alveolar bone resorption (P > 0.05).

This research established a murine model for HU and periodontitis, but based on micro-CT analysis of alveolar bone, no relationship between HU or UA levels and periodontitis was found.

To investigate the reciprocal causal relationships between periodontitis and hepatobiliary diseases through Mendelian randomization (MR) analyses, to provide evidence for joint prevention and clinical decision-making in patients with concurrent periodontitis and hepatobiliary diseases.

Single nucleotide polymorphisms (SNPs) were extracted from the largest genome-wide association study on periodontitis (17 353 cases, 28 210 controls) and hepatobiliary diseases within the European ancestry and used as instrumental variables (IVs). The strength of the associations was examined by calculating the F-statistic. The SNPs significantly associated with the outcome were removed by scanning on Phenoscanner platform. Bidirectional causal associations between periodontitis and hepatobiliary diseases were estimated using inverse variance weighted (IVW), MR-Egger, and Weighted Median methods. The robustness of the findings was further verified through additional sensitive MR approaches, including Cochran’s Q statistic（IVW）, Rucker’s Q statistic（MR-Egger）, MR-PRESSO and Leave-one-out analysis. Further MR analyses, utilizing other available genome-wide association studies (GWAS) on hepatobiliary diseases, were conducted to validate the results.

The IVW method found that periodontitis had a causal impact on acalculous cholecystitis (odds ratio = 1.277, 95% CI 1.097-1.485, P=0.002), implying an increased risk of acalculous cholecystitis associated with periodontitis, while the MR-Egger regression and Weighted Median failed to observe significant causal effects of periodontitis on acalculous cholecystitis. However, no bidirectional causal associations between periodontitis and nonalcoholic fatty liver disease, cirrhosis or liver cancer were observed using IVW, MR-Egger regression and Weighted Median. The bidirectional causal relationships were deemed unlikely to be influenced by horizontal pleiotropy. Further, the validation analysis based on alternative GWAS data suggested parallel results.

The MR analyses suggest that periodontitis may elevate the risk of acalculous cholecystitis. Further investigations, including clinical studies and mechanistic explorations, are warranted to validate these findings. However, the MR analyses do not support bidirectional causal associations between periodontitis and nonalcoholic fatty liver disease, cirrhosis or liver cancer.

To evaluate the bidirectional association between periodontitis and Sjögren’s syndrome using the Mendelian randomization (MR) method.

Genome-wide association study (GWAS) data of periodontitis (N = 45563) and Sjögren’s syndrome (N = 214435) were selected to meet the requirements of the same ethnicity and different regions.Inverse variance-weighted (IVW), MR-Egger, and weighted median (WM) tests were used to evaluate the causal effect. Cochran's Q statistics, MR-Egger intercept, MR-PRESSO and leave-one-out analysis were used as sensitivity analyses to assess the stability and reliability of the results.

After screening, the GWAS data of Sjögren’s syndrome were based on the Finnish region, and the periodontitis GWAS data were based on the UK region, both of which originated from European ancestry. Using IVW (OR = 1.017, 95% CI = 0.956-1.082), MR-Egger (OR =0.985, 95% CI= 0.956-1.082), and WM (OR =1.021, 95% CI = 0.948-1.099), no causal effect of Sjögren’s syndrome on periodontitis was found using any of the three methods. Conversely, no causal effect of periodontitis on Sjögren’s syndrome was found (IVW, OR = 1.024, 95% CI = 0.852-1.230; MR-Egger, OR = 0.978, 95% CI = 0.789-1.212; WM, OR= 1.024, 95%CI = 0.846-1.260). The sensitivity analyses indicated that the results were stable and reliable. Cochran’s Q test and MR-PRESSO revealed that there was no significant heterogeneity among the instrumental variables, which included single nucleotide polymorphisms (SNPs). The intercept of MR-Egger regression indicated no pleiotropy in the included SNPs. No individual SNP was found that significantly affected the results using the leave-one-out method.

This study does not support a bidirectional causal effect between periodontitis and Sjögren’s syndrome.